Aromasin the same as arimidex?

atali

Harem P.I.M.P
Hi bros! just need to know three things:
is aromasin the same a arimidex?
Will it hinder gains? (discovered myself that nolva DOES)
and at what dosage should be sufficient? they are 25 mg, was thinking a half tablet/day cuz these babies are EXPENSIVE
 
They are different drugs, but they are both aromatase inhibitors. It is like the differece Prozac and Paxil, which are both SSRIs.

I heard something recently that Aromasin doesn't damage the lipid panel like Arimidex and Femara (Letrozole). I can't confirm that, however.

Femara (Letro) has a stronger track record for reversing gynecomastia, but that doesn't mean that Arimidex or Aromasin won't work.
 
Mranak is onto something here. Some of the studies I have seen show that aromasin is not at tough on lipids as l-dex or letro. It seems to be a stronger Aromatase inhibitor (AI) than l-dex, almost rivaling letro. I have even read claims that aromasin can be used during post cycle therapy (pct), but I can't speak on that. I feel that using any Aromatase inhibitor (AI) during post cycle therapy (pct) is potentially a problem, but think l-dex is fine for the first two weeks of post cycle therapy (pct). But then again, that is just me....based on what I have seen with my own body.
 
In terms of the arimidex/aromosin/letro being harsh on your lipid profile, this study points to the fact that aromasin is bad and arimidex is good. There are so many contradictions in the research it's hard to figure out what is what.

Pharmacology and pharmacokinetics of the newer generation aromatase inhibitors.

Buzdar AU.

Department of Breast Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA. abuzdar@mdanderson.org

The newer generation aromatase inhibitors (AIs) as a class show efficacy and tolerability benefits over previously established treatments in postmenopausal women with advanced breast cancer. At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41-48 h, 2-4 days, and 27 h, respectively. Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have only been reported with exemestane. Anastrozole treatment has no impact on plasma lipid levels, whereas both letrozole and exemestane have an unfavorable effect. From indirect comparisons, anastrozole shows the highest degree of selectivity compared with letrozole and exemestane, in terms of a lack of effect on adrenosteroidogenesis. To date, there are no data suggesting any major differences in clinical efficacy between the newer generation AIs anastrozole and letrozole. Based on the observed pharmacological profiles, however, it cannot be assumed that the AIs will display the same tolerability and safety profiles when given for extended periods of time in the adjuvant setting. The effects of anastrozole, letrozole, and exemestane are being investigated in the adjuvant setting, and these data will elucidate the possible long-term consequences of the pharmacological effects reported after short-term exposure.

Publication Types:
Review
Review, Tutorial

PMID: 12538502 [PubMed - indexed for MEDLINE]
 
Aboot: thank you for posting this information.

The thing is, I thought that the damage to the lipid profile was caused by the lowered estradiol itself and not the drugs. But I haven't researched this; I need to look into it.

For now, I guess we'll all have to depend on our own bloodwork. Unfortunately, my lipid profile has been bad at least since the first lipid panel I had done when I was a teenager (total cholesterol over 300 even then).
 
mranak said:
The thing is, I thought that the damage to the lipid profile was caused by the lowered estradiol itself and not the drugs. But I haven't researched this; I need to look into it.

For now, I guess we'll all have to depend on our own bloodwork. Unfortunately, my lipid profile has been bad at least since the first lipid panel I had done when I was a teenager (total cholesterol over 300 even then).

Yeah, there is so much contradictory scientific information out there about this subject it is hard to know what is what. Like you said, if possible it is best to have your own blood work done and see how you are reacting to things as an individual.
 
Aboot said:
In terms of the arimidex/aromosin/letro being harsh on your lipid profile, this study points to the fact that aromasin is bad and arimidex is good. There are so many contradictions in the research it's hard to figure out what is what.

Pharmacology and pharmacokinetics of the newer generation aromatase inhibitors.

Buzdar AU.

Department of Breast Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA. abuzdar@mdanderson.org

The newer generation aromatase inhibitors (AIs) as a class show efficacy and tolerability benefits over previously established treatments in postmenopausal women with advanced breast cancer. At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41-48 h, 2-4 days, and 27 h, respectively. Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have only been reported with exemestane. Anastrozole treatment has no impact on plasma lipid levels, whereas both letrozole and exemestane have an unfavorable effect. From indirect comparisons, anastrozole shows the highest degree of selectivity compared with letrozole and exemestane, in terms of a lack of effect on adrenosteroidogenesis. To date, there are no data suggesting any major differences in clinical efficacy between the newer generation AIs anastrozole and letrozole. Based on the observed pharmacological profiles, however, it cannot be assumed that the AIs will display the same tolerability and safety profiles when given for extended periods of time in the adjuvant setting. The effects of anastrozole, letrozole, and exemestane are being investigated in the adjuvant setting, and these data will elucidate the possible long-term consequences of the pharmacological effects reported after short-term exposure.

Publication Types:
Review
Review, Tutorial

PMID: 12538502 [PubMed - indexed for MEDLINE]

I do not think it's fair to compare postmenopausal women with close to zero estrogen levels and male steroid users.

/Bruce
 
Bruce Banner said:
I do not think it's fair to compare postmenopausal women with close to zero estrogen levels and male steroid users.

/Bruce


Yeah, but we work with what we got. Outside of anecdotal information we get from each other (and ourselves) we have to work with the studies that are conducted. It's rare when a study is conducted for things that we are interested in using healthy males, let alone steroid users.
 
Bruce Banner said:
I do not think it's fair to compare postmenopausal women with close to zero estrogen levels and male steroid users.

/Bruce


Bruce, please post up any studies on the subject that you may have. I'm with Aboot, they will prove extremely difficult to find. Besides that, they would most likely contradict one another as well.

I think the only sure fire way to know what's going on is to have constant blood work done.
 
mranak said:
Don't pick on Mr. Benner too hard. He made a good point, but of course do did Aboot. We should take these studies for what they are worth.


Huh?

No one's picking on no one, just trying to keep the discussion going and search out any new studies, Bruce hangs on some European boards, and who knows, they might have stuff over there we never seen yet.
 
Shit, my bad. I could have sworn you wrote something different than what I am now reading you wrote. Too much on my mind today.

I'm certainly interested in any further information. In particular, I want to know if low estradiol by itself typically damages the lipid profile.
 
StoneColdNTO said:
Bruce, please post up any studies on the subject that you may have. I'm with Aboot, they will prove extremely difficult to find. Besides that, they would most likely contradict one another as well.

I think the only sure fire way to know what's going on is to have constant blood work done.

I agree that it's hard to find good information, but from what I can se the health issues using aromataste inhibitors is real and should be taken seriosly.

Quote Karl Hoffman:
While standard blood tests can detect detrimental changes in cholesterol profiles, studies in animals using aromatase inhibitors have demonstrated a rapid progression of atherosclerotic plaques. To my knowledge there is no way to test for this except via angiography, which would be too invasive to be performed routinely. Even an MRA, which is less invasive than a standard angiogram still employs contrast material and is quite expensive and has much lower resolution."

Testosterone inhibits early atherogenesis by conversion to estradiol: Critical role of aromatase
Localized Expression of Aromatase in Human Vascular Tissues
-------------------------------------------------------------

Not very pleasent reading

Endogenous Estrogens Influence Endothelial Function in Young Men.

Lew R, Komesaroff P, Williams M, Dawood T, Sudhir K.

Baker Medical Research Institute and Alfred Hospital, Prahran, Victoria, Australia, and Department of Medicine, Stanford University, Stanford, Calif.

Males produce endogenous estrogen from testosterone via the enzyme aromatase. Previous studies have suggested a role for endogenous estrogens in cardiovascular function in men. We examined the effects of endogenous estrogen suppression via aromatase inhibition on endothelial function, systemic arterial compliance, and lipoprotein levels in healthy young men. Using a placebo-controlled double-blind randomized design, 20 healthy men, aged 18 to 32 years, were randomized to receive either the aromatase inhibitor anastrozole (1 mg) or matching placebo. Hormone, lipid levels, C-reactive protein (CRP), and homocysteine were measured. Endothelial function, determined by flow-mediated dilation of the brachial artery, and systemic arterial compliance were assessed at baseline and after 6 weeks of treatment. There was a significant decrease in 17beta-estradiol concentrations with aromatase inhibition, from 85.4+/-4.2 to 64.3+/-8.1 pmol/L (mean+/-SD, P=0.042). Compared with baseline, a significant decrease in flow-mediated dilation was observed in subjects taking anastrozole [median, 6.1% (range, 5.2 to 13.4) to 3.5% (2.0 to 5.7), P=0.034] but not in the placebo group. No changes were observed in nitroglycerin-induced endothelium-independent dilation in either group. There was no change in systemic arterial compliance with either aromatase therapy or placebo. There were no significant changes in lipoproteins, testosterone, DHEA, CRP, or homocysteine levels in either the anastrozole or placebo group. We conclude that suppression of endogenous estrogens with an aromatase inhibitor resulted in impairment of flow-mediated dilation without significant changes in lipoproteins, homocysteine, or CRP. Our results suggest that endogenous estrogens play a direct regulatory role in endothelial function in young healthy men.

/Bruce
 
I think it is a good idea to simply keep estradiol are resonable levels until we have better information to figure all of this out. But keep bringing in all of these studies and whatnot. If we have to wait for a formal study on post-adolescent men, then we may be waiting a long time.
 
shleprock said:
What about using arimidex and letro at first signs of gyno for a couple weeks. would this be safe?
If the gyno came from estrogens, then one could use Nolva as a first line of defense.

There is no reason to use Arimidex _and_ Femara (Letrozole). Use one of them at a resonable, which keeps your estradiol at resonable levels, and you should be okay. We can make pretty good guesses about resonable dosages, but the only way to know the proper dosage for sure if to get a sensitive assay for serum estradiol.
 
i appreciate all the input bros but i dont think i got thr right answer yet..so arimidex and aromasin is not the same right? but is aromasin as effective? i noticed they are 25mg and adex ix only 5mg or something??
 
atali said:
i appreciate all the input bros but i dont think i got thr right answer yet..so arimidex and aromasin is not the same right? but is aromasin as effective? i noticed they are 25mg and adex ix only 5mg or something??
The simple answer is that all of the aromatase inhibitors: Arimidex (Anastrozole), Femara (Letrozole) and Aromasin (Exemestane) are all very effective at reducing serum estradiol. Thus, they all help with bloat, prevention of gyno. Each one has a different appropriate dosage, but no matter.

Now, Letrozole does seem more effective at doing things such as getting rid of existing gyno or damaging the lipid profile.

Most of our experience is with Arimidex and Femara. I have heard good things about Aromasin, but the number of people that use Aromasin is very small compared to the number of people that use Femara and Arimidex.

Really though, 1mg of Arimidex is _roughly_ equivalent to 25mg of Aromasin.
 
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